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W3: Disorders of Childhood

Disorders of Childhood Key words:

Attention Deficit Hyperactivity Disorder (ADHD)

Autism Spectrum Disorder Intellectual Disability

Neurodevelopmental disorders Dopamine

Inattention Hyperactivity Impulsivity

Psychostimulant medication Ritalin

DEX/ATX

Cognitive training

Echolalia Theory of Mind Sally Anne task Eye tracking studies Synaptic pruning

Applied behaviour analysis (ABA) antipsychotic medication

Down Syndrome Fragile X syndrome Williams syndrome

Fluorescent In Situ Hybridization (FISH) Elastin

Neurodevelopmental disorders

ONSET = developmental period, usually before child starts school Characterised by developmental deficits in:

Personal, social, academic and/or occupational functioning Often co-occur, can be specific impairment OR global (across domains) Not just deficits and delays – also behaviours in excess

Impulsivity – e.g. talking over the top of other people

Symptoms can be the same across different diagnosis- for example, attention difficulty is common in down syndrome, adhd etc

ADHD

Behavioural disorder – INATTENTION, HYPERACTIVITY and IMPULSIVITY

Onset – before 12yrs (Half are diagnosed before 6yrs - more severe= easier to recognise) 9 is the mean age.

For a diagnosis – must occur across domains (e.g. school, home) Must differ from normal at that age

Adults only need to show symptoms in 5 domains (6 for kids)

Prevalence = variable data bc diagnostic critea (DSM-IV vs ICM etc), different funding models (require diagnosis for funding) and location BUT no evidence that it is

increasing

More common in boys than girls.

Research not as common in girls-more research has been done into boys with ADHD Lifelong – symptom severity decreases tho – perhaps learnt to deal with symptoms

e.g. Adults with ADHD have jobs BUT lower SES and change jobs more often Causes

Heritability estimates of 70-80% from adoption and twin studies.

A single gene is unlikely to account for ADHD-Interaction of different genes, and environment – most likely.

But dopamine (receptor and transporter genes) seem to be involved

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W3: Disorders of Childhood

Early birth

Neurobiological: Smaller dopaminergic areas, less activation in frontal areas, reduced brain volume, delayed maturation etc

Environmental: Maternal smoking, alcohol use, maternal stress, low birth weight, nutritional, exposure to lead or pesticides, family adversity or low income

Treatment

Psychostimulant medication: Methylphenidate/Ritalin, Dexamphetamine (DEX), Atomoxetine (ATX)

Effective in the short term.

Have been used for more than 50 years.

Effective in reducing aggressiveness and impulsivity.

Cognitive training – rather than symptom focused – focused on the underlying cause. e.g. running everyday – improves cardiovascular system.

Parent training and change in classroom management- points system, understanding Intensive behaviour treatment

Autism Spectrum Disorder (ASM)

Lifelong developmental condition

Triad of impairment: SOCIAL AND EMOTIONAL DISTRUBANCE, COMMUNICATION DEFICITS and REPETITIVE/RITUALISTIC ACTS

Echolalia: repeat words or phrases over and over Repetitive act (speech)

Deficits in social communication/interaction

Eye tracking studies – ASM spend less time looking at other peoples faces.

Theory of mind – understanding the thought process of someone else.

Deficit in ASD

Sally Ann task – kids with ASM cant recognise that sally doesn’t have the info to know the marble is in the white box.

Increase in diagnosis…Why? broader criteria, more awareness and schools mandated to provide special services

More common in boys Causes:

Premature birth, older fathers – may be linked to ASM.

Increase in early brain growth – problem with Synaptic pruning? might not happen as effectively in ASM – over or under activation

Connectivity and/or abnormal cortical organization in frontal & limbic areas Siblings show more ASD symptoms (without meeting criteria) = genetic

Treatment

Applied behaviour analysis (ABA): intensive operant conditioning

operant conditioning – Teaching kids how to behaviour is certain social environments and rewarding the good behaviour.

Medication – not so effective, not first choice

BUT antipsychotic medication common – can help with comorbid factors

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W3: Disorders of Childhood

Treatment for symptoms e.g. sleep (melatonin) and anxiety Intellectual disability

Deficits in intellectual and adaptive functioning ONSET: during development (<18yrs)

Genetic or chromosomal abnormalities:

Down Syndrome

Fragile X syndrome: most common, high comorbidity with ADHD & ASM.

More common in males (XX vs XY female)

Williams syndrome: deletion of multiple genes on chromosome 7, distinct facial and social phenotype (increased approach to unfamiliar people)

Diagnosed through Fluorescent In Situ Hybridization (FISH)-gene present o no

Elastin–reduced levels in Williams syndrome – can cause problems with the organs. E.g. triple bypass surgeries by the time they’re 10.

large part of IQ testing=verbal- WS high verbal functioning but ID in other areas.

Treatment

Residential treatment (require extra care)

Cognitive treatment – strategies to solve problems, computer-assisted programs Behavioural treatments – Early intervention, small sequential steps, teach routines

Summary

ADHD: persistent inattention and/or hyperactivity and impulsivity. More frequent/severe than children of the same age

Autism Spectrum Disorder: Difficulty relating to others, communication and repetitive behaviours. Begins early, diagnosis has risen in recent years.

Intellectual disability: Deficits in intellectual functioning and adaptive behaviour.

Onset=during course of development.

Referensi

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